Background. Posttransplant lymphoproliferative disorders (PTLDs) occur after solid organ transplantation. Treatment guidelines include reduction in immunosuppression (RIS), radiation, rituximab, chemotherapy, and immunological agents. We present a rare case of recurrent diffuse large B-cell lymphoma presenting as a PTLD in a heart transplant patient treated with autologous blood stem cell transplant (ASCT) after failure of conventional therapy. Case Presentation. A 66-year-old male presented with a neck mass. He has a history of Hodgkin's disease status after staging laparotomy with splenectomy and heart transplantation due to dilated nonischemic cardiomyopathy 8 years prior to the development of PTLD. His examination was remarkable for right submandibular swelling. An excisional biopsy confirmed the diagnosis of diffuse large B-cell NHL. Patient received RIS, rituximab, chemotherapy, and radiation therapy with a complete remission. His lymphoma relapsed and he subsequently was treated with RICE salvage chemotherapy and consolidative high-dose chemotherapy with BEAC regimen followed by ASCT resulting in a complete remission. Conclusion. Patients with PTLD present a difficult therapeutic challenge. In this case, the patient's prior history of Hodgkin's disease, splenectomy, and a heart transplant appear to be unique features, the significance of which is unclear. ASCT might be a promising therapy for patients with relapsed or refractory PTLD.

This paper focuses on the development of a passive, lightweight skin patch sensor that can measure fluid volume changes in the heart in a non-invasive, point-of-care setting. The wearable sensor is an electromagnetic, self-resonant sensor configured into a specific pattern to formulate its three passive elements (resistance, capacitance, and inductance). In an animal model, a bladder was inserted into the left ventricle (LV) of a bovine heart, and fluid was injected using a syringe to simulate stoke volume (SV). In a human study, to assess the dynamic fluid volume changes of the heart in real time, the sensor frequency response was obtained from a participant in a 30° head-up tilt (HUT), 10° HUT, supine, and 10° head-down tilt positions over time. In the animal model, an 80-mL fluid volume change in the LV resulted in a downward frequency shift of 80.16 kHz. In the human study, there was a patterned frequency shift over time which correlated with ventricular volume changes in the heart during the cardiac cycle. Statistical analysis showed a linear correlation \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{upgreek} \usepackage{mathrsfs} \setlength{\oddsidemargin}{-69pt} \begin{document} }{}${R} ^{2} = 0.98$ \end{document} and 0.87 between the frequency shifts and fluid volume changes in the LV of the bovine heart and human participant, respectively. In addition, the patch sensor detected heart rate in a continuous manner with a 0.179% relative error compared to electrocardiography. These results provide promising data regarding the ability of the patch sensor to be a potential technology for SV monitoring in a non-invasive, continuous, and non-clinical setting.

Although the numbers are small, these data strongly suggest that there is an increased mortality risk for cardiac transplant recipients with prior HD who have undergone splenectomy.

Peripheral artery disease (PAD) is a condition caused by atherosclerotic blockages in the arteries supplying the lower limbs and is characterized by ischemia of the leg, progressive myopathy, and increased risk of limb loss. The affected leg muscles undergo significant changes of their biochemistry and metabolism including variations in the levels of many key proteins, lipids, and nucleotides. The mechanisms behind these changes are poorly understood. The objective of this study was to correlate the severity of the PAD disease stage and associated hemodynamic limitation (determined by the ankle brachial index, ABI) in the legs of the patients with alterations in the biochemistry of chronically ischemic leg muscle as determined by ATR‐Fourier transform infrared micro‐spectroscopy. Muscle (gastrocnemius) biopsies were collected from 13 subjects including four control patients (ABI≥0.9), five claudicating patients (0.4 ≤ ABI<0.9), and four critical limb ischemia (CLI) patients (ABI<0.4). Slide mounted specimens were analyzed by ATR‐Fourier transform infrared micro‐spectroscopy. An analysis of variance and a partial least squares regression model were used to identify significant differences in spectral peaks and correlate them with the ABI. The spectra revealed significant differences (P < 0.05) across control, claudicating, and CLI patients in the fingerprint and functional group regions. Infrared microspectroscopic probing of ischemic muscle biopsies demonstrates that PAD produces significant and unique changes to muscle biochemistry in comparison to control specimens. These distinctive biochemical profiles correlate with disease progression and may provide insight and direction for new targets in the diagnosis and therapy of muscle degeneration in PAD.